ABSTRACT
Hypoxia in surface waters driven by warming climate and other anthropogenic stressors is a major conservation concern, and technological solutions for water quality remediation are sorely needed. One potential solution involves the use of low-intensity electromagnetic fields (EMFs) to increase dissolved oxygen levels, but potential collateral effects of the EMFs on aquatic animals have not been formally evaluated. We examined the effects of EMF exposure on wild-caught, captive sunfish (Lepomis spp.) over 8-day and 3-day exposures, with and without aeration in mesocosms and stock tanks (respectively). We also quantified ambient fish abundance in close proximity to EMF devices deployed in Opinicon Lake (ON). We found no significant differences in a suite of blood-based stress physiology biomarkers, behaviors, and putative aerobic capacities between EMF and control conditions over 8 days. Aerated mesocosms equipped with activated EMFs consistently had higher oxygen levels in the water than aerated controls. There were no differences in mortality during 3-day oxygen depletion trials under EMF or control conditions, and we detected no differences in fish abundance when the devices were activated in the lake. Our findings suggest that deploying EMF devices in field settings is not likely to exert negative effects on exposed fish populations. PRACTITIONER POINTS: Low-cost, low-energy technological solutions to remediate aquatic hypoxia are sorely needed Electromagnetic fields (EMFs) can increase oxygen flux across air/water interfaces and increase dissolved oxygen levels We found no evidence of negative effects of EMFs on fish physiology or behavior and our results support their use in alleviating hypoxic conditions.
Subject(s)
Electromagnetic Fields , Oxygen , Animals , Fishes , Fresh Water , HypoxiaABSTRACT
It has been reported that Northern populations are exposed to mixtures of various environmental contaminants unique to the Arctic (Northern contaminant mixtures - NCM) at a large range of concentrations, depending on their geological location, age, lifestyle and dietary habits. To determine if these contaminants may contribute to a cardiovascular health risk, especially when combined with a high fat and sugar diet and ethanol exposure, we treated human coronary artery endothelial cells (HCAEC) with two mixtures of 4 organic (NCM1) or 22 organic and inorganic (NCM2) chemicals detected in Northerners' blood during 2004-2005 in the presence or absence of low-density lipoprotein (1.5mg/ml), very-low-density lipoprotein (1.0mg/ml) and glucose (10mmol/L) (LVG), and in the absence or presence of 0.1% ethanol. After 24h of exposure, cell morphology and markers of cytotoxicity and endothelial function were examined. NCM1 treatment did not affect cell viability, but increased cell size, disrupted cell membrane integrity, and decreased cell density, uptake of small peptides, release of endothelin-1 (ET-1) and plasminogen activator inhibitor (PAI), while causing no changes in endothelial nitric oxide synthase (eNOS) protein expression and nitric oxide (NO) release. In contrast, NCM2 decreased cell viability, total protein yield, uptake of small peptides, eNOS protein expression, and NO release and caused membrane damage, but caused no changes in the secretion of ET-1, prostacyclin and PAI. The presence of LVG and/or alcohol did or did not influence the effects of NCM1 or NCM2 depending on the endpoint and the mixture examined. These results suggested that the effects of one or one group of contaminants may be altered by the presence of other contaminants, and that with or without the interaction of high fat and sugar diet and/or ethanol exposure, NCMs at the concentrations used caused endothelial dysfunction in vitro. It remains to be investigated if these effects of NCMs also occur in vivo.
